Dose- and time-related changes in aerobic metabolism, chorionic disruption, and oxidative stress in embryonic medaka (Oryzias latipes): underlying mechanisms for silver nanoparticle developmental toxicity.

Silver nanoparticles (AgNPs) are widely employed in commercial products, and are thus inevitably released into the aquatic environment. Many studies have indicated that AgNPs could induce toxicological effects on embryonic fish. To understand the mechanism of AgNP developmental toxicity, we determined the effects of AgNPs on the egg membrane, aerobic metabolism, antioxidant system, lipid peroxidation, as well as reactive oxygen species (ROS) and singlet oxygen ((1)O(2)) generation in early-life medaka fish (Oryzias latipes). AgNP treatment at 62.5-1000 μg/L caused significant increase in retarded development and abnormalities. Destruction of the surface ornamentation and egg envelope was observed at a higher AgNP concentration (≥125 μg/L) using light microscopy and scanning electron microscopy. A dose-dependent increase in lactate dehydrogenase activity, an indicator of anaerobic metabolism, and superoxide dismutase activity was observed in the treated embryos. In contrast, the total reduced glutathione level decreased. A high thiobarbituric acid reactive substance concentration was generated upon AgNP exposure from day 1 to day 7 postfertilisation. The biochemical parameters suggested that oxidative stress was induced by the AgNPs. Unexpectedly, a dose-dependent reduction in ROS and (1)O(2) generation upon high AgNP exposure (≥250 μg/L) was observed. Although the morphological damages induced by the AgNPs were irreversible, restorable antioxidant defenses were noted in the well-developed embryos. This finding supported the idea that the stage of morphogenesis and organogenesis is a critical window to chemical exposure or environmental stress. Overall, the results suggested that hypoxia, disturbed egg chorion, and oxidative stress are mechanistically associated with AgNP toxicity in embryonic fish.